ABSTRACT
Eight stress-susceptible and eight normal pigs were used in the first portion of the study. Urine samples were collected for 24 hr over 4 consecutive days while the pigs were kept in metabolism cages. Each 24-hr sample was assayed for epinephrine, norepinephrine and dopamine. Urinary levels of dopamine were lower (P < .01) in the stress-susceptible pigs. No significant differences in urinary epinephrine or norepinephrine were observed. The second portion of the study evaluated the catecholamines in the caudate nucleus of the brain. Six stress-susceptible and six control pigs were examined. Immediately after exsanguination, caudate nuclei were excised and frozen in liquid nitrogen. The caudate nuclei were assayed for catecholamines within 2 to 3 days of freezing. Caudate nuclei dopamine levels were lower (P < .01) in stress-susceptible pigs (5,961 ng/g) than in control pigs (10,878 ng/g). No significant differences in norepinephrine levels of the caudate nuclei were observed between the two groups.
Subject(s)
Catecholamines/analysis , Caudate Nucleus/analysis , Stress, Physiological/veterinary , Swine Diseases/metabolism , Swine/metabolism , Animals , Creatine Kinase/blood , Dopamine/urine , Epinephrine/urine , Malignant Hyperthermia/blood , Malignant Hyperthermia/metabolism , Malignant Hyperthermia/urine , Malignant Hyperthermia/veterinary , Norepinephrine/urine , Stress, Physiological/blood , Stress, Physiological/metabolism , Stress, Physiological/urine , Swine/blood , Swine/urineABSTRACT
Malignant hyperthermia is a life-threatening complication of general anesthesia. Its cause is not precisely known but it appears to be related to a genetic defect that allows increased release or decreased reaccumulation of calcium by the sarcoplasmic reticulum whech then results in a hypermetabolic state. As with any unexpected complication when a patient is under general anesthesia, early diagnosis and treatment are essential. The early clinical signs that the surgeon and anesthesiologist shoulc be alert to are unexplained tachycardia, unexplained tachypnea, muscular rigidity, and increased temperature. Therapy should be accurate and immediate. The essentials of therapy are discontinuance of the anesthetic agent; immediate, active, and aggressive cooling; administration of procaine or procaine amide, 1 mg/kg/min until the pulse slows; correction of electrolyte and acid-base imbalances; maintenance of urinary output with furosemide and large volumes of fluids, intravenously; and supportive care. A thorough knowledge of the management of malignant hyperthermia ahd the pathophysiology of the complications that may occur with general anesthesia will allow the oral surgeon to fully meet his obligations to his patients.
